ACE inhibition delays development of terminal renal failure in the presence of severe albuminuria

Verseput, Gaico H.; Koomans, Hein A.; Braam, Branko; Weening, Jan J.; Provoost, Abraham P.

doi:10.1016/s0272-6386(00)70327-1

Cited by 13 publications

(12 citation statements)

References 24 publications

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“…Male FHH rats die of ESRF within a year and a half if not treated. [10,11] The FHH strain is well characterized by numerous physiologic and histologic studies [12][13][14][15][16][17][18][19]. Crosses between FHH and the proteinuria-resistant August × Copehnagen Irish (ACI) rat revealed the presence of five quantitative trait loci (QTLs) linked to UPV and other parameters of renal damage.…”

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confidence: 99%

Interaction between Rf-1 and Rf-4 quantitative trait loci increases susceptibility to renal damage in double congenic rats

Dijk

Specht

Lutz

et al. 2005

Kidney International

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confidence: 99%

Interaction between Rf-1 and Rf-4 quantitative trait loci increases susceptibility to renal damage in double congenic rats

Dijk

Specht

Lutz

et al. 2005

Kidney International

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“…[7][8][9][10][11][12][13] ACE inhibition has been reported to reduce glomerular capillary pressure, lower renal vascular resistance, and improve or preserve both renal blood flow and glomerular filtration rate. [7,14] The aim of our study was to compare the effects of the AT 1 receptor blocker, Irb, and the ACE inhibitor, Q, in STZ-induced diabetes in rats by assessing nephron function, renal morphology, and renal TGF-β 1 expression. We also determined whether combined use of Q and Irb is superior over the use of these agents alone.…”

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confidence: 99%

Effect of Angiotensin-Converting Enzyme Inhibition and Angiotensin II Type 1 Receptor Blockade on Streptozotocin-Induced Diabetic Nephropathy

et al. 2008

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The aim of this study was designed to investigate the possible beneficial effects of the angiotensin-converting enzyme (ACE) inhibitor, Quinapril (Q) and, the angiotensin (ang) II T 1 (AT1) receptor blocker, irbesartan (Irb), in streptozotocin (STZ)-induced diabetes in rats. The rats were randomly allotted into one of five experimental groups: A (control), B (diabetic untreated), C (diabetic treated with Q), D (diabetic treated with Irb), and E (diabetic treated with Q&Irb), each group containing 10 animals. Groups B-E received STZ. Diabetes was induced in four groups by a single intraperitoneal (i.p) injection of STZ (50 mg/kg, freshly dissolved in 5 mmol/L citrate buffer, pH 4.5). Two days after STZ treatment, development of diabetes in four experimental groups was confirmed by measuring blood glucose levels in a tail vein blood samples. Rats with blood glucose levels of 250 mg/dL or higher were considered to be diabetic. The rats in Q-, Irb-, and Q&Irb-treated groups were given Q (in a dose of 3 mg/kg body weight), Irb (5 mg/kg body weight), and Q&Irb (in a dose of 1.5 mg/kg + 2.5 mg/kg body weight) once a day orally by using intra-gastric intubation for 12 weeks starting two days after STZ injection. Treatment of Q and especially Irb reduced the glomerular size and thickening of capsular, glomerular, and tubular basement membranes; and increased amounts of mesangial matrix and tubular dilatation and renal function as compared with diabetics untreated. Notably, the better effects were obtained when Q and Irb given together. We conclude that Q, Irb, and especially Q+Irb therapy causes renal morphologic and functional improvement after STZ-induced diabetes in rats. We believe that further preclinical research into the utility of Q and Irb treatment, alone or its combination, may indicate its usefulness as a potential treatment in diabetic nephropathy (DNp).

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“…Indeed, there have been many studies both in humans and experimental animals detailing the benefits of ACE inhibition on kidney function 1–7 . Angiotensin‐converting enzyme inhibition has been reported to reduce glomerular capillary pressure, lower renal vascular resistance and improve or preserve both renal blood flow and glomerular filtration rate 1,8 …”

Section: Introductionmentioning

confidence: 99%

“…[1][2][3][4][5][6][7] Angiotensin-converting enzyme inhibition has been reported to reduce glomerular capillary pressure, lower renal vascular resistance and improve or preserve both renal blood flow and glomerular filtration rate. 1,8 Decreases in renal filtration surface area have been linked to elevations in mean arterial blood pressure, glomerular pressure and subsequent glomerulosclerosis. [9][10][11] Hence, it is likely that ACE inhibitors, through preventing pathological changes in glomerular structure, can maintain glomerular capillary length and, thereby, renal filtration surface area, thus preventing the vicious cycle of glomerular loss and progressive renal disease.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin‐converting enzyme inhibition in adult hypertensive rats: A stereological study of renal filtration surface area

Dunstan

Briscoe

Bertram

et al. 2003

Clin Exp Pharma Physio

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1. Angiotensin-converting enzyme (ACE) inhibitor treatment leads to beneficial effects on kidney function. The aim of the present study was to determine whether ACE inhibition at high or low doses affects glomerular capillary surface area and length, glomerular number or total renal filtration surface area in rats with established hypertension and, if so, to determine whether these effects are mediated through bradykinin potentiation. 2. Spontaneously hypertensive rats (SHR) were treated with the ACE inhibitor perindopril at either 3 or 0.1 mg/kg per day (high and low doses, respectively) from 16 to 24 weeks of age. Some rats were concomitantly treated with the bradykinin B2 receptor antagonist S16118 (10 nmol/kg per day). Blood pressure was measured twice weekly during the treatment period. At 24 weeks of age, rats were perfusion fixed at 140 mmHg, the kidneys removed, embedded in resin and examined stereologically to estimate glomerular number and volume, length and surface area of glomerular capillaries and total renal filtration surface area. 3. High- and low-perindopril treatment significantly reduced systolic blood pressure compared with control SHR. However, the rats treated with low-dose perindopril were still considered hypertensive. Neither low-dose nor high-dose perindopril treatment had any observable effect on glomerular number (23 876 +/- 1201 vs 26 240 +/- 1465 glomeruli/kidney, respectively) or volume (2.25 +/- 0.21 and 1.96 +/- 0.06 x 10-3 mm3, respectively) compared with controls (glomerular number 25866 +/- 1210 glomeruli/kidney; glomerular volume 2.24 +/- 0.21 x 10-3 mm3). As a result, there was no significant difference in total renal filtration surface area between any of the experimental groups (8161.6 +/- 550.9, 8699.7 +/- 427.6, 9081.9 +/- 453.6, 8830.2 +/- 521.2 and 8559.4 +/- 341.4 mm2 for SHR, SHR low-dose perindopril, SHR low-dose perindopril + B2 antagonist, SHR high-dose perindopril and SHR high-dose perindopril + B2 antagonist, respectively). Coadministration of the bradykinin antagonist had no observable effect on any of the parameters studied. 4. In conclusion, because neither high-dose nor low-dose perindopril had any effect on total renal filtration surface area, the observed beneficial effects of ACE inhibition on kidney function are not the result of enhancement in glomerular capillary surface area.

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ACE inhibition delays development of terminal renal failure in the presence of severe albuminuria

Cited by 13 publications

References 24 publications

Interaction between Rf-1 and Rf-4 quantitative trait loci increases susceptibility to renal damage in double congenic rats

Interaction between Rf-1 and Rf-4 quantitative trait loci increases susceptibility to renal damage in double congenic rats

Effect of Angiotensin-Converting Enzyme Inhibition and Angiotensin II Type 1 Receptor Blockade on Streptozotocin-Induced Diabetic Nephropathy

Angiotensin‐converting enzyme inhibition in adult hypertensive rats: A stereological study of renal filtration surface area

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